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OBJECTIVE Data about GnRHa on adult height in girls with central precocious puberty (CPP) have shown variable results, ranging from improvement of growth prognosis to lack of any benefit. This study was designed to delineate the criteria to decide which girls with idiopathic CPP (iCPP) will have a height benefit from GnRHa treatment. DESIGN Retrospective PATIENTS: 102 girls with iCPP who had reached final height (FH) were included. MEASUREMENTS Auxological, hormonal and radiological findings at treatment onset, and FHs were extracted from records. RESULTS Most important factor affecting height gain was chronological age (CA) at treatment onset. All the girls treated ≤6.4 years of age achieved a height gain of ≥1SDS, while none of the girls treated ≥8.3 years of age made the target. 75.6% of patients who started GnRHa between the ages of 6.4 and 8.3 years had a height gain of ≥1SDS. Most important factors affecting height gain in those treated 6.4-8.3 years were advanced bone age (BA), basal estradiol (E2 ) and pubertal stage (r2 : 0.906; P

OBJECTIVES The aims of this study were to describe changes in height during childhood and to investigate potential changes in the proportion of children attaining final height in childhood and in correlations between child and adult height across birth cohorts. METHODS We included 363 059 children (179 906 girls) from the Copenhagen School Health Records Register, who were born between 1930 and 1989, with height measurements at ages 7, 10, or 13 years. Linkages to data resources containing adult height values between ages 18 and 69 years were possible for a subpopulation of 96 133 individuals (23 051 women). Birth years were categorized as 1930 to 1939, 1940 to 1949, and 1950 to 1989. Descriptive height statistics were estimated by birth years and birth cohorts. Height correlations were examined using sex- and age-specific partial Pearson correlation analyses and meta-regression techniques. RESULTS Across 60 birth years, mean child heights at age 7 increased by 2.9 cm in girls and 3.0 cm in boys, and adult heights increased as well. The proportions of children attaining final height by age 13 remained low across the birth cohorts; nonetheless, there was a significant increase from 0.7% to 1.5% in girls only (P

AIM We analysed near final height (NFH) data in children with growth hormone deficiency (GHD) treated with recombinant human GH (rhGH). METHODS We divided the idiopathic GHD patients into two groups, isolated GHD (IGHD) and multiple pituitary hormone deficiency, to evaluate NFH. Then, data were grouped according to gender, pre-pubertal/pubertal status and spontaneous or induced puberty. The trial was performed as a retrospective study. Median values are given, and measurements are expressed as standard deviation scores (SDSs). RESULTS rhGH therapy was started at a median age of 12.1 (range 9.1-14.9) years in the IGHD group (n = 162, 83 males) and 9.1 (range 4.9-13.4) years in the multiple pituitary hormone deficiency group (n = 33, 22 males) at a median dose of 0.20 mg/kg/week. Height SDSs at the onset of therapy were -3.2 (range -4.4 to -2.6) and -3.9 (-6.8 to -2.8) in the two groups, respectively (P

This study investigated whether substantial body mass index (BMI) reductions in Swedish schoolchildren aged seven years to 19 years, caused by disease, healthy or unhealthy behaviour, had any impact on their final height.We used height and weight data on 6572 subjects from two nationally representative longitudinal samples of Swedish children born in 1973 and 1981. These provided information on their final height and any BMI reduction episodes.Of the 6572 subjects (50.9% boys), among individuals with information on final height, 1118 had a BMI reduction of 5% and10%, and 346 had at least one substantial BMI reduction of 10% or more. On a group level, there was no statistically significant difference in the final height of individuals with BMI reductions of 10% or more and those without. The findings were independent of age and the subject's BMI at the start of the reduction episode. However, there were a number of cases where a substantial BMI reduction probably had an impact on the subject's final height.Our study found no evidence that a substantial BMI reduction had any impact on final height on a group level, but further analyses of specific case studies are necessary to determine whether substantial BMI reduction might have an impact on final height.

Improvements in socioeconomic conditions in the 20th century resulted in earlier pubertal maturation in children and greater body height during childhood and adulthood (1).However, in some countries the positive secular changes that resulted in greater height, especially in the last decade of the 20th or in the early 21st century (2,3), have come to a halt. We previously reported a secular trend was still taking place in young men in Greece, but at a lower rate than the one recorded in the last quarter of the 20th century (4). The last study on the final height of Greek girls was performed in 2000-2001 and showed a positive secular change of 2.5cm (5) from the previous study performed about 20 years earlier (6). This article is protected by copyright. All rights reserved.

Aphrons are surfactant-stabilized microbubbles with thick soapy shells. Colloidal gas aphrons (CGA) with an average diameter of 50 μm have some unique properties: a high interfacial area due to their small size, a thick soapy shell and, above all, high stability compared to conventional foams. Various factors that can influence the performance of CGA dispersion, such as the type and concentration of surfactant, mixing time and processing parameters, have already been extensively studied. However, although CGA applications in various fields continue to advance, the influence of the disk diameter and baffle position of the aphron generator on the performance of CGAs has not been well studied. In this experimental work, the influences of the spinning disk diameter and baffle position inside the aphron generator have been investigated. Analyzing the drainage curve of various experimental runs revealed that the disk diameter and baffle position might have a positive impact on the stability of CGA dispersion particularly when the generation time or surfactant concentration is low. The experimental findings have been supported by other techniques such as half-life time and a new stability index, T 0.1, the time elapsed when the drained liquid from CGA dispersion reaches ten percent of its final height.

There are few data about the impact of cystic fibrosis-related diabetes (CFRD) on growth. We analyzed 17 children with cystic fibrosis (CF) presenting with newly diagnosed CFRD during puberty, in comparison with a matched control group of 52 CF children with normal glucose tolerance (NGT). Anthropometric evaluation showed that body mass index at CFRD diagnosis was significantly reduced in children with CFRD, in comparison with children with NGT (CFRD: -0.48 ± 1.08 vs. NGT: 0.2 ± 0.99; P=0.01), and the same difference remained evident at the end of follow up (CFRD: -0.49 ± 0.95 vs. NGT: 0.13 ± 0.89; P=0.04). Height standard deviation score (SDS) at baseline was slightly but not significantly lower in CFRD children (CFRD: -0.71 ± 0.83 vs. NGT: -0.25 ± 1.08; P=0.08), while final height SDS was significantly reduced (CFRD: -1.61 ± 1.12 vs. NGT: -0.61 ± 1.15; P=0.003). Mean final height SDS of the whole group was lower than mean target height SDS (final height SDS: -0.86 ± 1.2 vs. target height SDS: -0.3 ± 0.85; P

We report long-term, including final height, auxological data from our retrospective study of non-irradiated survivors of childhood acute lymphoblastic leukaemia (ALL). Body mass index (BMI) standard deviation score (SDS) increases in females, due to increased weight-SDS, persisted to final height, with probable adverse long-term health outcomes. In contrast, males demonstrated increased BMI-SDS in follow-up, due to reduced height-SDS, not increased weight-SDS, but such changes had resolved by final height. Childhood ALL survivors, particularly females, are therefore at potential increased risk of developing the metabolic syndrome during follow-up. We recommend that strategies to minimize weight gain should be implemented during ALL treatment.

The exon-3 deletion polymorphism (d3, Database of Genomic Variants ID: Variation_64191) in the growth hormone receptor (GHR) gene is associated with increased growth response to growth hormone (GH) therapy in GH-deficient patients. However, an association of the GHR genotype with height has not yet been reported in Prader–Willi syndrome (PWS). The aim of this study was to assess the association of GHR alleles with height before starting GH therapy in patients with PWS. Seventy-four patients with PWS were genotyped and their medical records were retrospectively reviewed (45 males and 29 females, median age 8.7 years). One hundred normal controls, with known final height, were also genotyped. The GH-exon 3 locus was genotyped using a PCR multiplex assay. The distribution of alleles in the patients with PWS was not different from controls [(fl/fl n = 53 (72%), fl/d3 n = 21 (28%)) in PWS vs. (fl/fl n = 72(72%), fl/d3 n = 26(26%), and d3/d3 n = 2(2%)]. However, patients with PWS carrying a d3 allele had significantly greater height standard deviation scores (SDS) (P = 0.025) and higher insulin-like growth factor I (IGF-I) level (P = 0.041), although the age at the start of GH therapy, weight, BMI, and body fat were not different. The d3 allele was associated with height and IGF-I levels before GH therapy and suggests that even before GH therapy, d3 allele may influence height through GH secretion. © 2011 Wiley Periodicals, Inc.

This article examines the relationship between human growth, final height, and the environment in early nineteenth-century England.While the reasons for stuntedness are multifactoral and involve lack of nourishment and in utero conditions, we should also give emphasis to respiratory, gastro-enteric, and bone disease along with the inadequate and sometimes harmful arrangements for convalescence, involving opiates and inadequate rest. Hard work and prevailing social attitudes slowed recovery and affected limb and organ development.While survival chances may have improved, and indeed were enhanced by measures such as targeted poor relief, quality of life for infants and children remained low and had an influence on their height as adults.The bodies of surviving working-class children showed the burden of hard times.

Deer antlers offer a unique model for the study of tissue-specific stem cells and organogenesis, as antler stem cells are confined to the antlerogenic periosteum (AP), a tissue that can be readily located (overlying a frontal crest) and experimentally manipulated. AP consists of an upper fibrous layer and a lower cellular layer. Tissue transplantation and membrane insertion experiments demonstrated that antler formation is triggered by the interactions between AP and the overlying skin. Interestingly, fairly normal antlers can be induced to grow by an inverted AP implant (the AP cellular layer facing the skin) at an ectopic site, raising the question whether the initial inductive signal is derived from the fibrous layer or cellular layer or both. To answer this question, in this study we used eight sika deer stag calves and selected one side of future antler growth region for implanting inverted AP and the contralateral side for noninverted AP as the control. The results showed that implantation of the AP discs in an inverted orientation generated pedicles with final height (17 ± 5.1 mm), less than half the height of those formed from the noninverted AP implants (45 ± 11.7 mm). Critically, antler transformation was initiated from a shorter pedicle, which was formed from the region where the AP cellular layer was brought in close proximity to the overlying skin. Therefore, the AP cellular layer, as opposed to the AP fibrous layer, is likely to be the main source of the initial inductive molecules for antlerogenesis.

Aim: Extreme tall stature may lead to a variety of concerns in tall children and their parents, leading to requests for treatment to reduce final height in some children. This study reviews referrals for tall stature to a single pediatric endocrinologist and results of treatment over 25 years from 1980 to 2004. Methods: Diagnoses, heights, target heights and estimated final heights at presentation, and final heights and complications in treated patients, were examined by retrospective chart review. Results: Of 345 referrals, 244 (71%) were girls and 101 (29%) were boys. Of the 68 (19.7%) treated, 53 (78%) were girls and 15 (22%) were boys. Most children had familial tall stature. Treated children were tall for their already tall families. Treatment reduced final heights compared with estimated final heights by (mean +/− standard error of the mean) 4.2 +/− 0.5 cm (P = 0.001) in girls and 5.1 +/− 0.8 cm (P

Aim: To assess final height in children with growth hormone deficiency (GHD) treated with human recombinant growth hormone (GH). Methods: Final height data for 401 Swedish children with idiopathic GHD and treated with GH, included in KIGS (Pfizer International Growth Database) between 1987 and spring 2006, were analysed retrospectively. Data were grouped according to sex, age and severity of GHD. Height at entry into KIGS, at the onset of puberty and near final height were analysed between groups. Results: Groups were heterogeneous for GHD, which ranged from partial to severe. For all groups, mean final height corrected for mid-parental height was within the normal Swedish height range. In patients with severe GHD, mean final height was almost identical to mean normal Swedish height. About 16% of patients showed disproportionality (short legs) at final height and were significantly shorter than other patients. The parents of these children also demonstrated short stature. Conclusion: Children with idiopathic GHD receiving GH replacement therapy can achieve a final height that as a group is within the normal range and all achieve a height within their genetic potential.

Short children with normal GH responses to arginine-insulin provocation testing and various amounts of spontaneously secreted GH over 24 hours participated in an ongoing study with GH, 0.1 IU/kg/day. A total of 40 prepubertal children have been treated for 1 year. Their mean height velocity increased from 4.6 to 7.5 cm/year. The children with the slowest pretreatment height velocity showed the best increment. An inverse relationship was found between the endogenous GH secretion and the increment in growth; 80% of the children had an endogenous GH secretion of less than 300 milliunits/litre/24 hours, estimated as area under the curve above the calculated baseline. They all showed an increment in height above 2 cm. The remaining 20% all had an endogenous GH secretion of more than 300 milliunits/litre/24 hours, estimated as area under the curve above the calculated baseline, Twenty-four of the children were prepubertal for the following 4 years, and their GH therapy continued. Their Deight velocity changed from 4.2 cm/year before therapy to 8.1,6.7,6.0 and 4.9 cm/year for the 1st, 2nd, 3rd and 4th years on treatment. Many of them have passed their expected final height, but have still not stopped growing. Those children who were in early puberty when GH treatment started went into a rapid growth spurt and have now stopped growing. They have all reached but not improved their expected final height. In 15 of the children GH treatment was stopped after 1-3 years. Their mean height velocity for the first post-treatment year was 5.1 cm/year; thus, for the group as a whole no‘catch down’was observed. Of the 15 children, only 4 decreased in height velocity despite increasing age. Further studies on the long-term results of GH treatment in larger groups of short children are needed to verify the findings in this study.

Long-term follow-up of growth and development after acute lymphoblastic leukaemia (ALL) in childhood has previously been limited to the prepubertal period. This study describes pubertal growth, final height and the spontaneous secretion of GH in girls treated for ALL, including CNS irradiation with 24 Gy. Ten girls, treated earlier for ALL, experienced the menarche at a mean age of 12.2 years. This is significantly earlier than the mean for Swedish girls. Prepubertal growth was near normal after the end of therapy for leukaemia. Mean final height was -1.7 SD, which is 1.5 SD less than at onset and 1.0 SD less than 1 year after the end of treatment. Thirteen other girls had a blunted spontaneous secretion of GH, several years after treatment for ALL; there was no increase in GH secretion during puberty. These results suggest that girls who have been treated for ALL, including CNS irradiation, have a relative GH insufficiency. This insufficiency becomes obvious only when the girls cannot respond to the increased need for GH during the pubertal spurt.

Oestradiol stimulates growth and development in Turner's syndrome. Previous results with low-dose oestradiol on growth rate are reviewed. The effect of oestradiol in low concentrations on somatomedin generation, GH secretion and directly on osseous tissue, may explain the growth response. The observations presented here of 35 girls treated with 17-beta-oestradiol demonstrated a definite increase in growth rate in the first year of therapy. Bone maturation was accelerated, but a reduction in final height was not found.

Aim To assess whether children with Noonan syndrome on long-term growth hormone (GH) therapy improve their final height to near mid-parental height. Methods Twenty-five prepubertal children (13 girls) with Noonan syndrome (NS) were studied. A single clinician made the diagnosis based on clinical criteria. GH treatment started at an age ranging from 3.1 to 13.8 y and was continued for at least 2 y. Improvement or "gain" in final height (FH) was defined as either the difference between adult height SD scores (SDS) and pre-treatment height SDS (the childhood component of the Swedish reference) or height SDS compared to the Noonan reference. Results Ten children received a GH dose of 33 microg/kg/d (mean age at start 7.7+/-2.1 y, mean age at stop 17.6+/-1.7 y) and 15 received a dose of 66 microg/kg/d (mean age at start 8.6+/-3.3 y, mean age at stop 18.4+/-2.1 y). Eighteen out of 25 patients reached FH. A substantial improvement in FH of 1.7 SDS, equivalent to 10.4 cm compared to pre-treatment height, was observed. No significant difference was seen between the two GH doses. Females gained a mean height of 9.8 cm and males 1-13 cm (FH 174.5+/-7.8 cm vs mean adult height of 162.5+/-5.4 cm for males with NS) at final height. Moreover, 60% reached a mid-parental height of+/-1 SD. Conclusion GH treatment improves final height in patients with Noonan syndrome, with a mean gain of 1.7 SDS. The prepubertal height gain is maintained to final height and the children achieve a height close to their mid-parental height.

Aim: To determine whether children with psychosocial short stature attain their genetic height potential. Methods: We report on 18 children (10 girls, 8 boys) diagnosed by a multidisciplinary team as having psychosocial short stature. All the children had had some kind of change in their environment (9 were separated from their families), and increased their mean height velocity standard deviation score (SDS) from −0.7 (1.3) to +3.6 (4.8) (p > 0.005) as well as their height SDS from −3.0 (0.3) to −2.6 (0.9) in the first year after the change. All the patients were post-pubertal and had reached their near final height (mean age, 20.0 y; range, 16.0–23.3). Results: Only 3 out of 18 had a greater final height than the mid-parental target height, 14 out of 18 had a near final height within the mid-parental target range (95% tolerance limits of the mid-parental height (±2 SD =±10 cm). Nevertheless, mean final height expressed in height SDS for the whole group was significantly shorter with −2.4 SDS compared with the mean of the mid-parental target height of −1.5 SDS (p > 0.001). Surprisingly, initial catch-up growth did not correlate with final height attainment. Conclusion: The majority of patients will attain a stature within the range of mid-parental target height, although towards the lower limit of this range.

Aim To determine the natural growth pattern of Japanese children with Down's syndrome. Methods Longitudinal height data of 85 patients (43 males, 42 females) from birth to final height were analyzed. Based on these data, semi-longitudinal standard growth curves and height velocity curves for Down's syndrome were drawn. Results The means +/- SD of final height of males and females with Down's syndrome were 153.2 +/- 5.6 and 141.9 +/- 4.2 cm, respectively. They were -3.0 SD and -2.8 SD for Japanese standards. Mean peak height velocities were 8.9 and 7.5 cm y(-1), and the ages at peak height velocity were 11.6 and 10.2 y for males and females, respectively. Conclusion The mean height of patients with Down's syndrome was around -2 SD for normal children before puberty. Their pubertal growth spurt starts about 1 y earlier and their peak height velocity was about 1.3-1.4 cm shorter than for normal children.

UNLABELLED The aim of the study was to evaluate whether sex hormone replacement therapy adversely affected final height and body disproportion in thalassaemic boys and girls. Thirty-six patients with spontaneous (SP) or induced puberty (IP) were studied in order to define the pattern of height growth through three observations: the first (A) at the age of 7-9; the second (B) at onset of spontaneous or induced puberty; and the third (C) when final height was reached. We examined 14 females with SP (f-SP) and 8 with IP (f-IP); 7 males with SP (m-SP) and 7 with IP (m-IP). Girls with IP reached the same final height of girls with SP (f-IP 153.8 (4.3) versus f-SP 154.4 (5.5) cm); p > 0.05) close to target height (f-IP 155.9 (5.2) cm versus f-SP 155.5 (3.6) cm). Girls with IP reached the final height at older chronological age (CA) (17.0 (0.6) y) than girls with SP (CA of 15.3 (0.7) y), but at the same bone age (BA) (f-IP 15.1 (0.9) y versus f-SP 14.8 (0.6) y). There was no difference between the two groups for pubertal growth (f-SP 16.2 (7.7) cm versus f-IP 12.2 (7.4) cm (p > 0.05)) that was negatively correlated with both prepubertal growth and BA at onset of puberty in both groups. Values of sitting height (sds) with respect to BA (SHsdsBA) were not significantly different between the two groups, and showed a worsening from the first observation to final height, reaching values around -2 SD, in both groups. Values of subischial leg length (sds) with respect to BA (SLLsdsBA) were in the normal range at both observations in all girls. High serum ferritin levels were observed in both groups (f-SP 3189 (2296) ng/ml and f-IP 3998 (2545) ng/ml; p > 0.05). Also boys with induced puberty reached the same final height of those with spontaneous one (m-IP 160.9 (5.5) cm versus m-SP 161.8 (2.4) cm; p > 0.05), but it was lower than target height in both groups (m-IP 168.1 (4.1) cm versus m-SP 169.6 (3.2) cm). Boys with IP reached final height at CA of 18.6 (1.1) y slightly older than boys with SP (CA 17.2 (0.9) y), but at the same BA (m-IP 15.9 (1.5) y versus m-SP 16.3 (0.8) y). Pubertal growth values were significantly different between boys with SP 18.9 (5.3) cm and those with IP 13.8 (4.9) cm (p < 0.05), but they were negatively correlated with prepubertal growth values in both groups (m-SP r = -0.91; p < 0.002 and m-IP r = -0.51; p < 0.05). SHsdsBA showed a worsening from the first observation to final height, reaching values around -3 SD in both groups, while SLLsdsBA were always in the normal range in all patients. Serum ferritin levels were higher in boys with IP (3400 (1179) ng/ml) than in those with SP (2020 (496) ng/ml). CONCLUSIONS Our data showed that: (a) patients of both sexes with induced puberty reached the same final height of patients with spontaneous puberty; (b) all patients showed a body disproportion with truncal shortening and normal leg length that was more severe in boys of both groups at final height; (c) body disproportion was independent of pubertal or prepubertal period of greater height gain, suggesting that sexual steroids replacement therapy did not adversely affect either final height or body disproportion. Further studies, focused on the pathogenesis of the truncal shortening, are necessary in order to acquire more insight into the causes of this impairment.

Aim: Normal growth patterns are seen throughout the first decade in children with cystic fibrosis (CF). Growth in the second decade is, however, less satisfactory and may reflect pubertal delay. This study was performed to assess the extent of pubertal delay, to examine factors that influence the timing and magnitude of the pubertal growth spurt, and to establish whether the final height for most CF patients differed significantly from the normal population. Methods: Thirty subjects (16 male) attending a single centre were studied. Peak height velocity (PHV), final height and ages when achieved were compared with population norms. Outcome data were correlated with disease severity using Shwachman and Chrispin-Norman scores and forced expiratory volume in 1 s. Results: PHV was significantly later in both genders in this CF population compared with Tanner and Whitehouse standards: boys 14.6 y (95% confidence interval (95% CI) 12.4–16.8, p < 0.01) and girls 12.6 y (95% CI 10.5–14.7, p < 0.01). Mean PHV was also lower in both genders (boys 7.7 cm y−1 and girls 6.4 cm y−1, both p < 0.001). However, final heights did not differ significantly from Freeman standards (height standard deviation scores: males–1.2, females–0.1); 52% of final heights equalled or exceeded the mid-parental centile. Conclusion: CF patients showed suboptimal PHVs with a later pubertal growth spurt influenced by disease severity, but eventually achieved a normal final height.

Aim Published Growth studies from Latin America are limited to growth references from Argentina and Venezuela. The aim of this study was to construct reference growth curves for height, weight, body mass index (BMI) and head circumference of Colombian children in a format that is useful for following the growth of the individual child and as a tool for public health. Methods Prospective measurements from 27 209 Colombian children from middle and upper socio-economic level families were processed using the generalised additive models for location, scale and shape (GAMLSS). Results Descriptive statistics for length and height, weight, BMI and head circumference for age are given as raw and smoothed values. Final height was 172.3 cm for boys and 159.4 cm for girls. Weight at 18 years of age was 64.0 kg for boys and 54 kg for girls. Growth curves are presented in a ± 3 SD format using logarithmic axes. Conclusion The constructed reference growth curves are a start for following secular trends in Colombia and are also in the presented layout an optimal clinical tool for health care.

AIM: To provide growth and sexual maturation reference data for Moroccan children living in The Netherlands and to compare them with the reference data of children of Dutch origin. METHODS: Cross-sectional growth and demographic data were collected from 2880 children of Moroccan origin and 14,500 children of Dutch origin living in The Netherlands in the age range 0-20 y. Growth references for length, height, weight, weight-for-height, body mass index (BMI) and head circumference were constructed with the LMS method. Predictive variables for height and BMI were assessed by regression analyses. Reference curves for sexual maturation were estimated by a generalized additive model. RESULTS: Moroccan young adults were on average 9 cm shorter than their Dutch contemporaries. Mean final height was 174.7 cm for males and 161.3 cm for females. Height differences in comparison with Dutch children increase from 2 y onwards. Height SDS was predominantly associated with target height. Compared to Dutch children, maturation started 0.2 and 0.9 y later for girls and boys, respectively. Median age at menarche was 12.9 y, 3.6 mo earlier than in Dutch girls (p = 0.001). BMI of Moroccan children was above that of Dutch children, especially for girls. BMI SDS was associated with birthweight in the age group 0 - < or = 5 y. CONCLUSION: Moroccan children living in The Netherlands are substantially shorter than Dutch children. Girls have higher weight-for-height and BMI for age. Median age at menarche occurs earlier. Given these differences, separate growth charts for the Moroccan children are useful.

Long-term outcome of growth and final adult height (FH) are a major concern of children after a renal transplantation (Tx). We therefore studied the yearly measurements of height (Ht), expressed as the Z-score and bone age (BA), in 58 children (28 girls) transplanted in our departments and followed-up for 5–18 (mean 9.6) yr after the operation. Twenty-four children reached final adult height. Renal function was evaluated as the glomerular filtration rate (GFR), which is estimated from the clearance of inulin. The mean Ht Z-score at Tx was −1.3 in girls and −2.7 in boys and increased to −0.6 and −1.5, respectively, at 5 yr after Tx. The greatest increase, seen in the shortest children and those transplanted before 7 yr of age, occurred during the first 3 yr. Children aged 7–12 yr at Tx showed an increase in height during the first years after the transplant, while those transplanted at >12 yr of age were not growth-retarded and therefore did not change their Ht Z-score. The most growth-retarded were also the most BA retarded. The mean FH Z-score was −1.1. A direct correlation was seen between GFR at 1 yr after Tx and the increase in height Z-score from Tx to 1 and 5 yr after Tx. In summary, the increment in height following Tx was the greatest in the most growth-retarded children and most marked during the first 3 yr after the transplant. FH was within normal range in 75% of the children. A high Ht Z-score at Tx had a positive effect on FH. Thus, growth after Tx was affected by the degree of stunting at Tx and renal function after Tx.

Summary objectives Constitutional delay in growth and adolescence (CDGA) is common in boys, some of whom request treatment to accelerate growth and attainment of secondary sexual characteristics. The aims of this study were to confirm that a 3-month course of intramuscular testosterone oenanthate does not impair final height in boys with CDGA, and to determine the accuracy of height prediction in this condition. design and patients Boys with CDGA who had attended the growth clinic, who were now at or close to final height and who had received either testosterone or declined treatment, were identified by retrospective case note analysis. Bone age assessment was carried out by a single observer, using the RUS (TW2) method of Tanner and Whitehouse. measurements The following auxological data were extracted from the case records: age, bone age, height, pubertal stage, parental heights and predicted final height. All subjects were then measured at age 19 years or greater. The main outcome measures were comparison of final height in treated and untreated boys; final height comparison with mid-parental height and with height prediction [RUS (TW2) method] at initial assessment and at subsequent review. results Sixty-four boys met the inclusion criteria, of whom 41 subjects had received testosterone and 23 were untreated. There were no significant differences between the groups (treated mean/SD vs. untreated mean/SD; P-value) in age (14·3/0·7 vs. 14·0/1·1; 0·13), height (144·7/6·2 vs. 144·2/6·2; 0·79), mid-parental heights (170·4/5·5 vs. 171·1/4·5; 0·59), and bone age (12·0/1·2 vs. 12·3/1·3; 0·36). Final heights in both groups (168·9/6·0 vs. 168·2/3·5; 0·65) were closely related to predicted final heights (170·0/5·0 vs. 168·1/4·1; 0·15) and only slightly less than mid-parental heights. Only three subjects had final heights below the initial height prediction range. conclusions Our data support the hypothesis that this treatment regime does not adversely affect the final height achieved in constitutional delay of growth and adolescence and that height prediction, assessed by a single observer, is a useful and accurate tool.

Summary objective The management of children with congenital adrenal hyperplasia (CAH) remains a challenge, especially with regard to growth potentials. The objective of our analysis was to uncover the factors that influence the growth and final height of patients with CAH. design The linear growth pattern and body mass index (BMI) at different developmental stages (birth to 2 years, 2 years to puberty initiation and puberty initiation to final height) and the final height achieved were analysed retrospectively in 48 patients with 21-hydroxylase deficiency; 17 with the salt-wasting (SW) form, 25 with the simple virilizing (SV) and six with the nonclassical (NC) form. results Mean final height (FH) and FH-SDS were, respectively, 170·8 ± 5·6 m and −0·57 ± 0·8 in males and 156·7 ± 6 cm and −0·61 ± 1 in females with the SW form, 166·1 ± 6·1 cm and −1·05 ± 1 in males and 151·6 ± 5·4 cm and −1·4 ± 1 in females with the SV form and 159·7 ± 6·9 cm and 0·3 ± 1·4 in females with the NC form. In subjects with the SW form, height SDS at 2 years, at puberty initiation and at FH were −0·18 ± 0·9, 0·11 ± 1·28 and −0·6 ± 1·0, respectively. FH achieved was not different from target height (TH) in the SW group, but it was significantly lower than TH in the SV group (P = 0·003). FH in the SW group showed a positive correlation to the height achieved at 2 years of age (r = 0·68, P = 0·019), and height at 2 years was negatively related to the hydrocortisone dose in the birth to 2-year period (r = −0·79, P = 0·011). FH showed no correlation to hydrocortisone dose at any of the three developmental periods studied. BMI-SDS were not different in the various forms of CAH and showed no correlation to FH or hydrocortisone dose. Age at menarche was comparable to that in our general population. conclusions Under our conditions of management, the final height of patients with the salt-wasting form was comparable to the target height and to the most favourable literature data. The patients with the simple virilizing form fare less well, mainly due to delayed diagnosis and consequent advancement of bone age and early puberty. In salt-wasting patients, height at 2 years is comparable to normals, it is influenced by the hydrocortisone dose and is related to the final height. Some height is lost during puberty. Hence, monitoring treatment over the first 2 years and during puberty is critical for the outcome in these patients.

OBJECTIVE Human GH treatment of patients with childhood-onset (CO) growth hormone deficiency (GHD) ceases when they reach final height; this provides an opportunity to retest GH status in all patients before determining whether GH therapy will be required in adult life. At present, the diagnostic approach to these patients is not fully standardized. This study aimed to characterize a large group of previously GH-treated CO GHD patients and establish their GH status. PATIENTS AND METHODS The multinational study included 167 patients diagnosed as GH deficient and treated with hGH to final height during childhood. Mean age was 19.2 years and mean height standard deviation score (SDS) was -1.08. Peak serum GH concentrations were determined in standard GH stimulation tests. IGF-I and IGFBP-3 concentrations were determined at a central laboratory and converted to SDS values by reference to a normal population. RESULTS Using only a peak GH value of less than 3 microg/l (1 mg = 3 U) in stimulation tests as the cut-off, 133 (79.6%) patients would be classed as GH deficient. Using only an IGF-I value less than -2 SDS as the cut-off, 134 (80.2%) patients would be classed as GH deficient. However, by using both criteria there were 120 (71.9%) patients who were definitely severely GH deficient (group 1) and 20 (12.0%) who were not GH deficient (group 2), leaving 14 (8.4%) classed as GH deficient from IGF-I SDS only (group 3) and 13 (7.8%) classed as GH deficient from stimulation test only (group 4). There was no difference between the groups in height SDS or body mass index (BMI), but the GH-deficient patients tended to have been diagnosed at a younger age (group 1, 8.2 +/- 3.9; group 2, 10.0 +/- 4.0; P = 0.052). For patients classed as GH deficient compared with those not GH deficient, the percentage of males was lower (group 1, 64.2%; group 2, 90.0%; P = 0.022) and the percentage with multiple pituitary hormone deficiencies was higher (group 1, 81.7%; group 2, 20.0%; P < 0 .001), with the other two groups being intermediate in each case. Only the group classed as GH deficient by both criteria had a mean IGFBP-3 less than -2 SDS and both IGF-I SDS and IGFBP-3 SDS increased steadily across the four groups. CONCLUSIONS A high percentage (71.9%) of these childhood-onset GH-deficient patients were still GH deficient in adult life and are likely to require further hGH treatment. While 12.0% could be classed as definitely no longer GH deficient, there are some patients who are intermediate (16.2%) and may be classed as GH deficient by one criterion but not the other. When GH stimulation test results and IGF-I concentration are discordant, the IGFBP-3 level does not establish diagnosis and the hGH treatment requirement of such patients remains a dilemma.

Purpose To examine final height in relation to target height in asthmatic patients with and without glucocorticoid treatment while growing up compared with healthy individuals. Methods In 1990 and 1993, questionnaires were distributed to all individuals born in 1974 and 1977 in the counties of Jamtland and Gastrikland in Sweden. All individuals reporting use of anti-asthmatic drugs or symptoms indicating possible obstructive airway disease, and a sample of healthy volunteers were invited to a clinical examination. Results Overall, 356 asthmatic patients and 384 healthy individuals were identified. In 1998–1999, all subjects were invited to a follow-up study and final height was analysed in relation to target height in 152 asthmatic patients and 131 healthy individuals. It was found that both men and women achieved a higher mean final height than the calculated mean target height. There were no significant differences between controls and asthma patients treated either with or without glucocorticoids. Most of the patients treated with glucocorticoids started their therapy during adolescence and 92% had used inhaled budesonide. There was no trend towards a decrease in final height in relation to target height when inhaled budesonide treatment was initiated prior to adolescence or with lifelong cumulative dose of inhaled budesonide. Conclusions Asthmatic adolescents treated with inhaled budesonide achieve normal final height in relation to their target height. Copyright © 2002 John Wiley & Sons, Ltd.

Objectives Within populations, height is positively associated with economic success and in economically developed populations inversely associated with health. Recent studies also suggest air pollution may result in higher bone turnover markers among children, which may affect growth. However, few studies have investigated the effect of air pollution on height or growth rate. We therefore assessed the associations of several air pollutants with height at different ages. Methods We simultaneously assessed associations of particulate matter with a diameter of 10 micrometers or less (PM10), sulfur dioxide (SO2), nitric oxide (NO), and nitrogen dioxide (NO2) in utero, in infancy, and in childhood with height at different ages (∼9, ∼11, ∼13, and ∼15 years), in a population-representative birth cohort “Children of 1997” (n = 8327) from the developed non-Western setting of Hong Kong with relatively high air pollution and short children, using partial least square regression. Results After considering multiple comparison, higher SO2 in childhood was associated with shorter height at ∼13 years (–0.20 cm, 99% CI −0.32 to −0.06). This difference was not evident at ∼15 years. Conclusions These observations suggest that air pollution may affect the trajectory of growth and development rather than final height, with corresponding implications for health in later life.

Objectives Eveleth and Tanner's descriptive documentation of worldwide variability in human growth provided evidence of the interaction between genetics and environment during development that has been foundational to the science of human growth. There remains a need, however, to describe the mechanistic foundations of variability in human height growth patterns. Methods A review of research documenting cellular activities at the endochondral growth plate aims to show how the unique microenvironment and cell functions during the sequential phases of the chondrocyte lifecycle affect long bone elongation, a fundamental source of height growth. Results There are critical junctures within the chondrocytic differentiation cascade at which environmental influences are integrated and have the ability to influence progression to the hypertrophic chondrocyte phase, the primary driver of long bone elongation. Phenotypic differences in height growth patterns reflect variability in amplitude and frequency of discretely timed hypertrophic cellular expansion events, the cellular basis of saltation and stasis growth biology. Conclusions Final height is a summary of the dynamic processes carried out by the growth plate cellular machinery. As these cell-level mechanisms unfold in an individual, time-specific manner, there are many critical points at which a genetic growth program can be enhanced or perturbed. Recognizing both the complexity and fluidity of this adaptive system questions the likelihood of a single, optimal growth pattern and instead identifies a larger bandwidth of saltatory frequencies for “normal” growth. Further inquiry into mechanistic sources of variability acting at critical organizational points of chondrogenesis can provide new opportunities for growth interventions.

Identification of subtle textural differences or changes in foods in isolation has been a difficult task because they are usually accompanied by differences or changes in other sensory properties. Textural modification of semi liquid foods can easily be produced by mechanical means without affecting their taste and appearance. The changes can be then quantified using squeezing flow viscometry without introducing new uncontrolled modifications. Comparison of the measurements with sensory evaluations of the same samples can establish the threshold of sensory detection, at least in principle. To test this hypothesis, the consistency of practically intact mayonnaise, tomato paste, yogurt and strawberry jam of two commercial brands each were evaluated by squeezing flow viscometry using an Instron UTM. Other samples of the same brands were stirred mildly to modify their consistency and then compared with the undisturbed samples. The textural differences were expressed in terms of the apparent stress at three compressed specimen heights, and the residual stress after 60 and 120 s at the final height. Relatively large differences, as judged by these mechanical measures were also detected by an untrained sensory panel, but the 'correct identifications' never reached a 100%. In the case of the two different brands of yogurt, the panel failed to establish the existence of differences, which were clearly detected by the instrument. This suggests that not every difference, detectable instrumentally, has a corresponding sensory response. Although the number of results in this preliminary work was too small to establish the exact threshold for sensory detection, the methodology seems to be appropriate for such a purpose. This is because of the high reproducibility of the squeezing flow parameters and their sensitivity to even subtle difference in the tested specimens consistency. La viscosimetrie en ecoulement lors de la compression d'echantillons de mayonnaise, de puree de tomate, de yaourt et de confiture de fraise est mesuree. Puis les echantillons sont remues doucement pour modifier la consistence et de nouvelles mesures sont faites. Les tests sont egalement effectues par un panel de degustateurs non entraines, qui sont capables de detecter des differences de textures entre les produits remues ou non. Le nombre de resultats obtenues dans cette etude ne permet pas de determiner le seuil sensoriel de detection d'une difference de consistance mais la methodologie est appropriee.

UNLABELLED It is well known that some adult diseases, such as cardiovascular diseases, may be programmed during foetal life. It is not clear, however, whether final height may be predicted from foetal growth. A longitudinal cohort of full-term healthy Swedish babies (n = 3,650) was followed up from birth to maturity in a population-based growth study. Length or height and its changes were analysed from birth to 18 y of age; 2,807 children, with data available on birth length, final height and parental height, were included in this analysis. The result clearly shows that length at birth relates to final height. In terms of standard deviation scores (SDS), the mean difference in length at birth from the mean was greatly decreased in final height, but retained the same order as was seen at birth. In terms of centimeter difference from the reference mean values, the difference in length at birth remained roughly stable into final height. For instance, babies 5 cm above or below the mean birth length will end up approximately 5 cm above or below the mean in final height. Parental height-a surrogate value of the genetic final height potential of an individual-is shown to influence postnatal growth in height strongly. However, the difference from the mean in length at birth remained into adulthood within the same midparental height group. CONCLUSION This study reveals that trends in foetal linear growth continue into maturity. Foetal growth is a significant predictor of postnatal growth. Final height is dependent on both the magnitude of foetal growth and the genetic potential in stature, and appears to some extent to be programmed from foetal growth.

To optimize growth hormone (GH) treatment in girls with Turner syndrome, two multicentre studies were carried out in The Netherlands: a frequency-response study (study 1) and a dose-response study (study 2). In study 1, 19 girls with Turner syndrome, aged 11 years or older, were treated with one or two daily injections of GH at a total dose of 6 IU/m2/day (0.067 mg/kg/day) and ethinyloestradiol given orally at a dose of 0.05 microg/kg/day. All the girls reached final height. The mean (+/-SD) gain in final height was not significantly different between the once- or twice-daily regimens (7.6 +/- 2.3 versus 5.1 +/- 3.2 cm, respectively). The mean final height attained was 155.5 +/- 5.4 cm. All the girls exceeded their adult height prediction. In study 2, 68 girls with Turner syndrome, aged 2-11 years, were randomized into three dosage groups: A, B and C. During the first year, the girls in all the groups received GH at a dose of 4 IU/m2/day (0.045 mg/kg/day), which group A continued to receive throughout the study. At the start of the second year, groups B and C were switched to a dose of 6 IU/m2/day, which the girls in group B continued to receive for the remainder of the study. At the start of the third year, the girls in group C were switched to a dose of 8 IU/m2/day (0.090 mg/kg/day) for the remainder of the study. After 7 years of GH treatment, height SDS (based on Turner syndrome and normal population references) increased significantly in all three groups, but significantly more in groups B and C compared with group A (p = 0.02 and p = 0.001, respectively). Predicted adult height increased significantly, without a significant difference between the three dosage groups. The mean final heights of 25 of the girls were 159.1, 161.8 and 162.7 cm for groups A, B and C, respectively.

OBJECTIVE Birth weight influences both postnatal growth and the initial response to GH therapy in GH-deficient subjects, but its relationship to final height is uncertain. Therefore, we examined final height results in a group of subjects treated for GH deficiency who were born small, appropriate or large for gestational age (GA). DESIGN Retrospective study. PATIENTS 108 GH-treated patients (age at diagnosis 11.1 ± 2.0 years) affected by idiopathic and isolated GH deficiency (peak

This study was conducted to analyse the effect of childhood-onset diabetes mellitus on adult height. The height at time of diagnosis of 35 children with insulin-dependent diabetes mellitus (IDDM) was compared with growth reference data. Predictions of the adult height were made at the time of diagnosis using the target height and the Tanner-Whitehouse II method. The adult height was compared with both the predicted values and the height of healthy adults. The height at time of diagnosis of the prepubertal children was increased compared with growth reference data, in contrast to pubertal children who had normal heights. Only the prepubertal boys were taller at time of diagnosis. The adult height of the prepubertal patients was taller than growth reference data. The mean adult height in all patients did not differ significantly from the predicted heights. In conclusion, the increased height at the start of IDDM in prepubertal children persists until adulthood.

Tanaka T, Satoh M, Yasunaga T, Horikawa R, Tanae A, Katsumata N, Tachibana K, Nose O, Hibi I. When and how to combine growth hormone with a luteinizing hormone-releasing hormone analogue. Acta Paediatr 1999; Suppl 428: 85–8. Stockholm. ISSN 0803–5326 The effect of combined treatment with growth hormone (GH) and a luteinizing hormone-releasing hormone (LHRH) analogue, or GH alone, on pubertal height gain was assessed in an uncontrolled study in 15 boys and 10 girls with GH deficiency (GHD). Seven boys and six girls were treated with GH alone (group 1), and eight boys and four girls were treated with a combination of GH and an LHRH analogue during puberty (group 2). Mean ages (□ SD) at the start of GH treatment and at the onset of puberty were significantly lower in group 2 (8.0 □ 3.3 years and 11.2 □ 0.8 years, respectively, in boys, and 6.3 □ 1.6 years and 10.8 □ 0.7 years in girls) than in group 1 (12.8 □ 1.9 years and 13.7 □ 1.4 years in boys, and 11.2 □ 1.0 years and 12.5 □ 1.2 years in girls). Height at the onset of puberty was less in group 2 than in group 1, but the difference was significant only for the boys. Combination treatment was started at a mean age of 11.7 □ 1.2 years in boys and 11.5 □ 1.0 years in girls. The duration of the combination treatment was 5.1 □ 1.5 years in boys and 2.3 □ 0.7 years in girls. The duration of the period between the onset of puberty and the end of GH treatment was significantly longer in group 2 (6.8 □1.2 years in boys and 5.5 □ 1.0 years in girls) than in group 1 (4.3 □ 1.6 years in boys and 3.6 □1.4 years in girls). The pubertal height gain was also significantly greater in group 2 (36.7 □ 6.5 cm in boys and 29.0 □ 8.3 cm in girls) than in group 1 (21.9 □ 4.1 cm in boys and 18.6 □ 4.1 cm in girls). Final height was significantly greater in group 2 than in group 1 in boys. Although there was no significant difference in final height between groups in the girls, the change in height SDS from the start of GH treatment until final height was significantly greater in group 2 (2.7 □ 1.6 in boys and 4.5 □ 0.5 SD in girls) than in group 1 (1.0 □ 0.8 in boys and 1.8 □ 0.9 SD in girls), in both boys and girls. In conclusion, it appears that combination of an LHRH analogue and GH may increase the pubertal height gain and the final height of children with GHD. The improvement is attributed to the prolongation of the treatment period, permitting slow bone maturation, and to the maintenance of height velocity. This combination treatment appears to be more effective in boys than girls. To fully assess this therapeutic approach, prospective controlled studies are needed. □Growth hormone deficiency, growth hormone treatment, luteinizing hormone-releasing hormone analogue, pubertal height gain

Final height was evaluated in 369 patients with idiopathic growth hormone deficiency (IGHD) enrolled in KIGS--the Pharmacia & Upjohn International Growth Database. At the start of growth hormone (GH) therapy, the patients were 9.8 years of age, their mid-parental height SDS was -0.8, and their height SDS was -3.1. Of the 369 patients, 50% had multiple hormone deficiencies, and puberty was induced in 31%. Patients were 18 years of age at completion of GH therapy, and had received GH at a dose of 0.49 IU/kg/week (0.16 mg/kg/week), with a mean of 5.2 injections/week for 8.1 years. Final height SDS was -1.5, final minus initial height SDS was 1.7 and final minus mid-parental height SDS was -0.5. A Swedish subgroup (n = 69) received conventional GH therapy throughout at 0.65 IU/kg/week (0.22 mg/kg/week), with seven injections/week for a mean of 9.4 years. These patients achieved their genetic potential (final minus mid-parental height SDS, 0.03), with a normal final height SDS of -0.3. For the total group, the following variables were associated with final height: mid-parental height SDS (r = 0.62), injection frequency (r = 0.37), duration of GH treatment (r = 0.28), peak stimulated GH concentration (r = -0.25), age (r = -0.19) (all p < 0.001) and height velocity SDS in the first year of treatment (r = 0.20, p = 0.004). In conclusion, genetic potential, expressed as the mid-parental height, is the variable with the greatest identified influence on final height during GH treatment in IGHD. Current GH regimens will lead to a normal height and attainment of mid-parental height. However, higher dose, individualized GH regimens are likely to be necessary for patients with IGHD who are disadvantaged at the time of commencing GH therapy, such as those with short parents, those whose treatment began in late childhood or adolescence and those with less severe GHD.

Background: Growth retardation following steroid treatment in children is a major problem. Reduction of steroid dose has been tried using immunosuppressive agents such as cyclosporine A or mizoribine in children with frequently relapsing nephrotic syndrome. Few reports concerning final height in steroid-sensitive nephrotic syndrome (SSNS) are available. Method: Patients who developed SSNS before 15 years of age and reached their final height were retrospectively studied by standard deviation score (SDS) of height and target height calculated by their parental height. Results: A total of 34 patients were evaluated for their final height. The mean age at onset of SSNS was 8.0 years and the mean age at last follow up was 21.6 years. In total, 22 patients had frequent relapses and were treated with cyclophosphamide, mizoribine or cyclosporin A. All patients had normal renal function at the last evaluation. The mean final height was 168 cm in males and 155 cm in females. The mean height SDS was 0.37 at the time of onset and was −0.43 when they reached their final height (P = 0.0001). The final height was a mean of 2.5 cm below target height and was significantly lower than their siblings (P = 0.007). Final height of two boys who continued to have frequent relapses during puberty and were not treated with cyclosporin A was 146 and 150 cm. Conclusion: Final height in children with SSNS was slightly affected by steroid treatment and two patients had severe growth retardation.

The aim of this work was to assess the outcome of recombinant growth hormone (rGH) therapy in a large unselected group (72) of patients with Turner's syndrome (TS), 26 of whom have reached final height. Growth data were collected from Scottish patients with TS and outcome was assessed in three ways: response to therapy in the first year, response in subsequent years and final height. Phenotypic, auxological, genetic and biochemical factors, all of which may have affected the first-year response, were investigated. Fifty-one percent of the cohort had a clinically "good" first-year response to therapy and 49% had a "poor" response, a "good" response was defined as a change in the TS standard deviation score (SDS) of +0.5 or more and a "poor" response as a change in the TS SDS of less than +0.5. The percentage of children showing a positive change in TS SDS after 2, 3 and 4 years of therapy declined (88%, 78%, 41%). Mean (range) final height was 142.6 (133.4-153.6) cm, mean (range) pretreatment TS SDS was -0.27 (-2.1 to +1.09) and mean (range) final TS SDS was -0.05 (-1.4 to +1.59). Thirteen (50%) patients attained a final height that was greater than projected, eleven did not attain their projected final height and two achieved their exact projected final height. Short girls with TS appear to benefit more from rGH supplementation than tall girls, but otherwise there was no significant correlation between any of the parameters studied and the response to treatment. It is concluded that large-scale prospective studies are still required to assess the impact of rGH on final height in TS and to identify factors responsible for the variability in response.

To determine how accurately the Roche-Wainer-Thissen (RWT), Tanner-Whitehouse (TW2), and Bayley-Pinneau (BP) prediction models estimated adult height, serial height predictions were made for 23 healthy boys (mean initial age 10.4 ± 1.1 years) every 8 months from 8-15 years of age. The RWT model was tested using Greulich-Pyle (RWT-GP) and Fels (RWT-Fels) bone ages. Stature was measured every 4 months until near final height was attained (growth rate

Accurate adult height prediction is of clinical importance in assessing the need for pharmacological intervention and in the evaluation of the outcome of therapy. The methods currently in use are subject to a wide range of error, one source of which is the use of bone age (BA) measurements. We have developed a computer model for predicting adult height in pubertal boys without using BA determinations. The model is based on the existing Infancy-Childhood-Puberty model and calculates the onset of the pubertal growth spurt. Predicted adult height was assessed using this new model and four others in a group of normal boys and in a group of short normal boys receiving growth hormone. Calculated final heights by all the methods were not significantly different. Incorporation of paternal height into the prediction equations increased the accuracy of the prediction. It was concluded that our new model is as accurate as existing methods of predicting final height that involve assessing BA.

These oestrogen-resistant and aromatase-deficient cases now establish a more complete picture of how androgen and oestrogen combine to regulate pubertal growth (47, 48) and demonstrate that oestrogen deficiency states need not be lethal (1). Whereas original concepts suggested that skeletal maturation and pubertal growth were attributable to androgen and, therefore, were not sexually dimorphic, current evidence preserves the notion of common mechanisms in both sexes, but points to oestrogen as the principal steroid involved in the final phases of skeletal maturation. Oestrogen can be viewed as a primary determinant of the final height of a child, in the sense that oestrogen initiates and completes epiphyseal closure. The full scope of the effects of androgen on epiphyseal maturation and linear height regulation is less clear but evidence suggests that androgen has direct and indirect effects through its aromatization to oestrogen (Fig. 2). Remarkably, under unusual circumstances, a rather prolonged period of continued growth can be achieved with minimal bone-age advancement, as long as oestrogen concentrations and/or sensitivity are low. Given this more complete understanding of the role of oestrogen, and with the availability of more sensitive assays for oestradiol (49), a new era in sex-steroid physiology and pubertal growth has been inaugurated (50). However, any therapies directed towards manipulating growth with sex steroids will need to take account of the possibility of untoward effects on other processes, such as the accretion of bone mineral mass (51,52).

Longitudinal records from 13,707 children (6749 boys and 6958 girls), aged 6-17 years, were fitted by a smoothing cubic spline function, and the factors influencing changes in height SD score (SDS) during puberty were analysed. Height SDS at 6 years correlated closely with final height SDS. However, short children at 6 years of age tended to increase their height SDS at final height, whereas tall children at the same age tended to decrease their final height SDS for children with the same prepubertal height, the later that pubertal maturation occurred, the greater was the final height achieved. As short children entered puberty relatively late and tall children entered puberty relatively early, height SDS tended to approach 0 SD during puberty. A prediction function obtained by multiple regression analysis using height SDS at 6 years, the percentage by which the child is overweight at 6 years, age at onset of the pubertal growth spurt (PGS) and height at onset of the PGS provides a reasonable model for the prediction of final height SDS without the need to estimate bone age.

Measurements of final height were made on more than 4000 children in the final grade of school in Gothenburg in 1992; at the same time, mid-parental heights were recorded. These data were combined with other information (sex, length of gestation, size at birth, estimated age at peak height velocity (PHV) and height measurements made before 8 years of age) and used in a multiple regression analysis to assess the strength of the linear relationship between attained final height and these other potentially predictive measures of adult height. The R2 value increased from 0.16 at birth to 0.64 when the child was 8 years old. The inclusion of mid-parental height in the regression analysis contributed significantly to the explained variation in final height, especially at the earlier ages; the further addition of size at birth and age at PHV provides a small increase in the explained variation. The probability that the final height of a child will be below -2 or above +2 standard deviation scores (SDS) was assessed, based on previous SDS values for height when younger and on mid-parental height SDS. As a result of the large sample size included in the analyses, considerable confidence can be placed on the accurate prediction of final height values in the range -2.5 to +2.5 SDS.

Achondroplasia, a form of short stature with short limbs, is the most common disease among osteochondrodysplasia. The growth pattern of patients with achondroplasia is unique compared with the normal standard. At birth, patients' heights are within normal limits and height velocity is normal during the first year in most patients. Thereafter, it declines to the 3 percentile line and remains low until 8 years of age. The peak height velocity is much lower during puberty in these patients than in the normal and contributes to short stature in achondroplasts. Extremely short stature lowers quality of life, therefore, various medications have been tried to promote growth in achondroplasts but in vain. GH is now produced in sufficient quantity utilizing recombinant DNA technique. Since encouraging results have been obtained in the GH treatment of various kinds of short stature without GH deficiency, e.g., Turner's syndrome, intrauterine growth retardation, non-endocrine short stature, etc., achondroplasia has been also considered as a candidate for GH treatment. There have been only a few studies on GH treatment in achondroplasia and the number of subjects studied is small. However, satisfactory growth-promoting effects have been demonstrated in these studies although observation periods were short and side effects have not been reported. Further studies are necessary to confirm the optimal dosage and administration method on final height and side effects in long-term use of GH.

The physiological control mechanisms underlying the histogenesis of the pedicle, which precedes antler growth, from the frontal bones of male deer are poorly understood. The aim of this study was to investigate the extent of pedicle/antler regeneration after removal (for histological evaluation) of the antlerogenic region or pedicle tissue during pedicle development to determine whether the subsequent pattern of regeneration could contribute to the understanding of pedicle histogenesis and the mechanism of the transition between permanent pedicles and deciduous antlers. The contralateral pedicles of six stags were not removed and these data serve as controls. All deer were observed frequently and measurements of regeneration were made in March after all antler growth had ceased for that season. The developmental stage of the pedicle was determined by a combination of pedicle height measurements and histological studies. The results showed that pedicle formation histologically covers three stages: a period of intramembranous ossification (when the pedicle is less than 5 mm in height), a period when the ossification pattern changes (when the pedicle is between 5 and 28 mm in height) and a period of modified endochondral ossification (when the pedicle is over 30 mm in height). In all ossification stages some deer regenerated neither antlers nor pedicles. The pedicles which regenerated following the loss of antlerogenic tissue at the intramembranous ossification stage were shorter than the controls (P < 0.01), but longer than the pedicles regenerated after pedicle removal at the transitional stage in the pattern of ossification (P < 0.01). No pedicle tissue was regenerated if the pedicles were removed at the endochondral ossification stage and antlers were directly formed from the deer's head. Thus the final height of the regenerated pedicles was closely linked with the histological ossification stage of the original pedicle at removal. Antler regeneration took place at all stages but two deer grew pedicles only when tissue removal took place during the transition period. Overall the results provide evidence that the potential to regenerate a pedicle diminishes as the pedicle increases in height and the necessity for pedicle growth to precede antler growth also decreases. The fact that some deer, whose tissues were removed at the transition period of ossification change, regenerated pedicles but failed to generate antlers highlights the importance of this stage for the transition between the permanent pedicle and the deciduous antler. The results provide evidence for an hypothesis that it is the transition between ossification types which signals the end of pedicle development and the onset of antler development. © Wiley-Liss, Inc.

Patients with Ullrich-Turner syndrome (UTS) are treated increasingly with growth hormone (GH) to improve growth velocity and final height. For evaluation of the effectiveness of this treatment, different methods have been applied and we demonstrate that the results depend, to some extent, on the specific method that has been used for analysis of data. We have analysed height and growth velocity data as well as the applied methodology from 13 studies on spontaneous growth in UTS. Most studies were based on calculations of annual means or medians of data collected in a longitudinal/cross-sectional manner; others used mathematical models. Growth velocities were calculated longitudinally in individual patients or were derived from height curves graphically or mathematically. Individual height data for a given age varied between 2.6 and 7.7 cm, when estimated annual means were applied, and between 0.4 and 5.8 cm when mathematical models were used. Reported data on growth velocity were almost identical in all studies except for the age of expected puberty, when some authors found a minor pubertal growth spurt. Standard deviations for growth velocity increased at the time of pubertal age and amounted to up to 70% of the respective growth velocity. When various UTS height standards were applied for evaluation of treatment effects, we found a difference of up to 100% of the SD score due to the different SD values of reference data. Results expressed as height SD score may be biased by relatively low mean heights of reference data at adolescent ages.

It is known what the aim is in a complete long-term growth study; the final height is the outcome measure, although the annual height velocity values provide additional information. Strictly, short-term growth studies are also defined in terms of minimum length of observation, i.e. one month, as well as the type of measurement errors to be considered. The poor correlation between short- and long-term growth velocity values has led to the conclusion that the short-term study cannot be interpreted in long-term perspectives, and vice versa. There is a need to debate the way in which results of short-term studies should be interpreted. This is especially important when short-term growth is taken as the outcome measure in a controlled study. Our proposal is that such studies must include information about the growth achieved for a period after the treatment has ended in order to describe possible compensatory growth. Without weighing in some long-term consequences, we may incorrectly document short-term growth as a positive or negative effect of a certain treatment.

Pubertal linear growth in 66 adopted Indian girls was studied. The infancy-childhood-puberty standard was used, since it is applicable to Indian girls, and enables determination of the onset and height gain of the pubertal growth phase in an individual. At arrival in Sweden, mean height was -2.8 SDS. Despite rapid catch-up growth, the girls were still below the reference mean (-0.8 SDS) at the onset of the pubertal growth spurt, which occurred approximately 1.5 years earlier than in Swedish girls and also earlier than in Indian girls. The pubertal height gain, however, was equivalent to that in Swedish girls with similar timing of puberty. The short final height found in some of these girls appears to be related to shortness prior to puberty and to very early onset of an otherwise normal pubertal growth component.

Eight children with congenital adrenal hyperplasia and late initiation of corticosteroid treatment are included in the present study. Four of them received LHRHa treatment for the arrest of central precocious puberty, while the other four served as controls. The administration of LHRHa was effective in arresting the manifestations of puberty. The final height in the LHRHa-treated group was 158.2 +/- 7.3 cm (SDS -1.1 +/- 0.5) and did not differ from the target height of 158.9 +/- 6.5 cm (SDS -1.1 +/- 0.2), while the final height in the controls was 153 +/- 11 cm, a value significantly lower than their target height of 164.5 +/- 8.3 (SDS -0.6 +/- 0.7) with p < 0.05. The data showed that LHRHa is effective in arresting central precocious puberty and appears to improve final height, bringing it closer to that expected from the genetic potentials.